As Mark Pallen points out, if mutations in rpoS are so common, why do
bacteria enduring long-term starvation acquire mutations in rpoS, that
confer some sort of advantage? I read a very recent article (Waterman,
SR and Small,PLC (1996) Infect Immun. 64 2808-2811) on an analysis of
a large number of shiga-like toxin producing strains of E. coli
(SLTEC), where they found that acid tolerance, which is dependent upon
sigma-s, is extremely variable between strains. Those strains which
are less tollerant to acid require a much higher infective dose than
the very acid tollerant strains. An examination of the less acid
tollerant strains revealed that these virulent strains have mutations
in rpoS. Thus, when we talk about some pathogens requiring a high
infective dose while others such as Shigella only require a couple of
cells to initiate disease, perhaps we should be considering the
functionality of the stationary phase regulon and the presence of rpoS
mutations, and correlate these with infectivity. Interestingly
therefore, it is not just in the laboratory stains that accumulate
these mutations, but in wild strains with teeth!